Cardiac decompensation generally refers to the failure of the heart to maintain adequate blood circulation due, for example, to HF or other medical ailments. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues. The build-up of fluids in the lungs due to poor heart function is referred to as cardiogenic PE. Herein, HF, CHF and cardiogenic PE are all considered to be cardiac decompensation events.
It is highly desirable to detect cardiac decompensation events within a patient and to track the progression thereof using implantable medical devices so that appropriate therapy can be provided. At least some techniques have been developed for detecting HF/PE events and delivering responsive therapy that exploit electrical impedance signals (or related signals such as admittance or immittance) measured within the patient.
See, e.g., U.S. Patent Application 2010/0069778 of Bornzin et al., entitled “System and Method for Monitoring Thoracic Fluid Levels based on Impedance using an Implantable Medical Device”; U.S. Pat. No. 7,628,757 to Koh, entitled “System and Method for Impedance-Based Detection of Pulmonary Edema and Reduced Respiration using an Implantable Medical System”; and U.S. Pat. No. 7,272,443 to Min et al., entitled “System and Method for Predicting a Heart Condition based on Impedance Values using an Implantable Medical Device.” See, also, U.S. patent application Ser. No. 11/558,194, of Panescu et al. filed Nov. 9, 2006, entitled “Closed-Loop Adaptive Adjustment of Pacing Therapy based on Cardiogenic Impedance Signals Detected by an Implantable Medical Device.” Still further, see U.S. Patent Application 2009/0287267 of Wenzel et al., entitled “System and Method for Estimating Electrical Conduction Delays from Immittance Values Measured using an Implantable Medical Device,” which described techniques for using impedance to evaluate conduction delays that can be converted to LAP values for tracking HF.
Although impedance-based HF/PE techniques are generally effective during a chronic implant phase beginning a few months after device implant, problems can arise during an acute phase during the first month or two following device implant. During the acute phase, the electrodes used by the device to detect impedance are subject to on-going tissue encapsulation. During that interval, changes in tissues surrounding the electrodes—including tissues surrounding the housing of the device itself—can greatly affect the impedance values measured using the electrodes, typically rendering impedance-based HF/PE detection systems unreliable and unusable.
In this regard, the human body typically encapsulates the leads and device during the first thirty to sixty days following the implantation. The encapsulation tissue changes the local impedance characteristics surrounding the lead electrodes, as well as the device housing electrode. It is now believed that the majority of the impedance characteristics occur within about one centimeter of the electrodes used to measure the impedance. Given that the majority of the signal occurs near the electrode and the encapsulation occurs on or near the surface of the electrode, it is expected that measured impedance signals will vary with changes in encapsulation. This applies to both transthoracic or intrathoracic impedance signals (measured between the device housing and electrodes on or within the heart) and intracardiac impedance signals (measured between a pair of electrodes on or within the heart.) Herein, transthoracic impedance signals are also referred to as “PE impedance signals,” since the transthoracic signals are used to detect PE. Intracardiac impedance signals are also referred to herein as cardiogenic impedance (CI) signals, since the intracardiac signals exhibit variations representative of the beating of the chambers of the heart.
Moreover, the magnitude and duration of changes to impedance during encapsulation can depend greatly on the individual patient's genetics, immune system, the health of the patient, the affects of the steroids, patient medications, and many other factors. Given all of these parameters, it is currently not feasible to determine a priori when impedance signals will stabilize. Therefore, at least some state-of-the-art HF/PE impedance detection systems are programmed to ignore the first forty-five days or so of impedance data, post-implant. That is, a moratorium is imposed within algorithms of the device against collecting impedance data during that initial interval for the purposes of detecting HF/PE. (Impedance may be measured for other reasons, such as to detect lead failure.) Furthermore, many HF/PE impedance detection systems employ a fourteen day moving average as a baseline for use in detecting HF/PE. Therefore, once the encapsulation process is complete, such systems need an additional fourteen days to fully stabilize before HF/PE detection can begin, which means that such systems do not detect or respond to cardiac decompensation events during the first sixty days after implant, leaving the patient potentially vulnerable. It is noted that not all devices ignore the first forty-five days of impedance data. Some devices may ignore only the first thirty days of data. Nor do all devices employ a fourteen day “moving average” window. Typically, though, HF/PE impedance-based detection systems are not activated until about forty-five to sixty days post implant.
It would be desirable to provide techniques for detecting HF, PE or other cardiac decompensation events that can be employed during the post-implant acute phase. It would also be desirable to determine within a particular patient whether impedance-based HF/PE detection systems can be safely activated before completion of the typical forty-five to sixty-day post-implant interval. It is to these ends that aspects of the present invention are directed.